Abstract

Telomeres, the tandem nucleotide sequences at the termini of the DNA, enables the masking of DNA from repair mechanisms, thus protecting them from being considered as double stranded breaks. When the maintenance of telomeres goes awry, several diseases including cancer are resulted. Here in this review, we give an account of how telomere shortening, lengthening, positioning in the nucleus and its associated epigenetic modifications set cancer cells apart from normal cells.